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This investigation compared percent fat obtained via underwater weighing using measured and predicted residual lung volume (RLV) in euhydrated and hypehydrated collegiate wrestlers (N = 67). RLV was measured using [O.sub.2] rebreathing or [0.sub.2] dilution and predicted using 3 equations--Equation 1:(0.019 x height [cm]) + (0.0115 x age [years])--2.24; Equation 2: (0.017 x age [years]) + (0.06858 x height [in.])--3.477; and Equation 3: (0.0275 age [years]) + (0.0189 height [cm])--2.6139. Percent fat determined using RLV Equation 2 did not differ from the value obtained using measured RLV in the euhydrated (10.9 (+ or -] 5.1 vs. 11.5 [+ or -] 5.6% fat) or hypohydrated (10.8 [+ or -] 5.1 vs. 12.3 [+ or -] 5.6% fat) trials. All other percent fat values differed (p < 0.05) from the value obtained using measured RLV in euhydrated subjects. The use of RLV Equation 2 may be a practical alternative to measured RLV in determining percent fat in euhydrated and hypohydrated collegiate wrestlers. KEY WORDS. percent fat, hydration status, hydrostatic weighing

Abstract: Objectives: Myofibroblasts (myoFb) are the major cell types that appear at the site of myocardial infarction (MI) in response to injury and play a vital role in tissue repair/remodeling. Since vascular endothelial growth factor (VEGF) plays a crucial role in the infarcted/ischemic heart, we hypothesized that activation of the peroxisome proliferator-activated receptor (PPAR)-γ by its agonists induces VEGF expression while simultaneously decreasing inflammation (NF-κB). Such an increase in myoFb VEGF expression by PPAR-γ agonists may play a role in angiogenesis. Methods: Rat myoFb were treated with PPAR-γ agonists and VEGF expression was measured by ELISA. The effect of these agonists on VEGF receptors was determined by qRT-PCR and flow-cytometric analysis. VEGF produced by these cells was also used for analysis of in vitro tubule formation (Matrigel assay). Results: The PPAR-γ activators troglitazone (TZ) and 15-deoxy-prostaglandin J2 (15J2) induced the expression of VEGF and its receptors (Flt-1 and KDR) in myoFb. TZ and 15J2 elicited a significant increase in the expression of KDR (14.7±1.0% and 9.6±2.1% respectively) and Flt-1 (24.5±2.0%, and 14.0±2.2% respectively) when compared to untreated myoFb. MyoFb treated with PPAR-γ agonists increased extracellular VEGF, augmenting tubule formation on a Matrigel. The PPAR-γ activator 15J2 significantly decreased the NF-κB activity in myoFb. Conclusion: This study demonstrates the induction of the VEGF accompanied by a reduction of NF-κB activity (inflammatory signaling) by PPAR-γ agonists in cardiac myoFb. These results may further the understanding of the beneficial effects of PPAR-γ agonists on infarcted tissue repair and angiogenesis. [Copyright &y& Elsevier]

The end-stage renal disease population poses a challenge for obtaining venous access required for life-saving invasive cardiac procedures. In this case report, we describe an adult patient with end-stage renal disease in whom the hepatic vein was the only available access to implant a single-lead permanent cardiac pacemaker. A 63-year-old male with end-stage renal disease on maintenance hemodialysis and permanent atrial fibrillation/atrial flutter presented with symptomatic bradycardia. Imaging studies revealed all traditional central venous access sites to be occluded/non-accessible. With the assistance of vascular interventional radiology, a trans-hepatic venous catheter was placed. This was then used to place a right ventricular pacing lead with close attention to numerous technical aspects. The procedure was completed successfully with placement of a single-lead permanent cardiac pacemaker.